The Emirates Mars Mission.

The Emirates Mars Mission (EMM) was launched to Mars in the summer of 2020, and is the first interplanetary spacecraft mission undertaken by the United Arab Emirates (UAE). The mission has multiple programmatic and scientific objectives, including the return of scientifically useful information about Mars. Three science instruments on the mission's Hope Probe will make global remote sensing measurements of the Martian atmosphere from a large low-inclination orbit that will advance our understanding of atmospheric variability on daily and seasonal timescales, as well as vertical atmospheric transport and escape. The mission was conceived and developed rapidly starting in 2014, and had aggressive schedule and cost constraints that drove the design and implementation of a new spacecraft bus. A team of Emirati and American engineers worked across two continents to complete a fully functional and tested spacecraft and bring it to the launchpad in the middle of a global pandemic. EMM is being operated from the UAE and the United States (U.S.), and will make its data freely available.

Short-Range Disorder in TeO2 Melt and Glass.

High-resolution X-ray pair distribution functions for molten and glassy TeO2 reveal coordination numbers nTeO ≈ 4. However, distinct from the known α-, ß-, and γ-TeO2 polymorphs, there is considerable short-range disorder such that no clear cutoff distance between bonded and nonbonded interactions exists. We suggest that this is similar to disorder in δ-TeO2 and arises from a broad distribution of asymmetric Te-O-Te bridges, something that we observe becomes increasingly asymmetric with increasing liquid temperature. Such behavior is qualitatively consistent with existing interpretations of Raman scattering spectra, and equivalent to temperature-induced coordination number reduction, for sufficiently large cutoff radii. Therefore, TeO2 contains a distribution of local environments that are, furthermore, temperature dependent, making it distinct from the canonical single-oxide glass formers. Our results are in good agreement with high-level ab initio cluster calculations.

Patterns of Nitrogen Excretion by Embryonic Softshell Turtles (Trionyx spiniferus) Developing in Cleidoic Eggs.

Embryonic softshell turtles develop inside eggs exchanging little, if any, liquid water with the nest environment. Despite the consequent restriction on availability of water to support development, embryos convert most of the ammonia released in catabolism of proteins into soluble urea rather than insoluble urate, and thereby commit a portion of their limited reserve of water to serve as solvent for metabolic wastes. This finding is contrary to expectations from prior studies of cleidoic eggs.

Possible adaptive value of water exchanges in flexible-shelled eggs of turtles.

Use of energy reserves by embryos of common snapping turtles (Chelydra serpentina) is related to the hydric conditions to which eggs are exposed during incubation and to the net exchanges of water through the eggshells. Embryos developing inside eggs with a relatively favorable water balance use more of their energy reserves metabolically and grow larger before hatching than embryos inside eggs with less favorable water exchanges.

Affective modulation of multiple memory systems.

The hippocampus and caudate nucleus are anatomical components of relatively independent memory systems and recent research has focused on the nature of the interaction between these two systems. The amygdala exerts a general modulatory influence on memory storage processes related, in part, to an organism's level of affective or emotional arousal. Moreover, affective state can influence the use of different memory systems, and the amygdala may mediate this effect of emotion on memory. Recent evidence indicates that the amygdala modulates the separate types of memory mediated by the hippocampus and caudate nucleus. Recent human brain imaging studies also point to both sex- and hemisphere-related asymmetries in amygdala participation in emotionally influenced memory.

Amygdala is critical for stress-induced modulation of hippocampal long-term potentiation and learning.

Stress is a biologically significant factor shown to influence synaptic plasticity and memory functioning in the hippocampus. This study examined the role of the amygdala, a brain structure implicated in coordinating stress behaviors and modulating memory consolidation, in mediating stress effects on hippocampal long-term potentiation (LTP) and memory in rats. Electrolytic lesions of the amygdala effectively blocked the adverse physiological and behavioral effects of restraint and tailshock stress, without impeding the increase in corticosterone secretion to stress. Physiologically, hippocampal slices from stressed animals exhibited impaired LTP relative to slices from unstressed control animals, whereas hippocampal slices from stressed animals with amygdalar lesions exhibited normal LTP. Behaviorally, stressed animals were impaired in retention of a hippocampal-dependent hidden platform version of the Morris water maze task, and this impairment was blocked by amygdalar lesions. In a fixed location-visible platform water maze task that can be acquired by independent hippocampal and nonhippocampal memory systems, stress enhanced the use of nonhippocampal-based memory to acquire the task. These results indicate that an intact amygdala is necessary for the expression of the modulatory effects of stress on hippocampal LTP and memory.

The Drosophila beta-amyloid precursor protein homolog promotes synapse differentiation at the neuromuscular junction.

Although abnormal processing of beta-amyloid precursor protein (APP) has been implicated in the pathogenic cascade leading to Alzheimer's disease, the normal function of this protein is poorly understood. To gain insight into APP function, we used a molecular-genetic approach to manipulate the structure and levels of the Drosophila APP homolog APPL. Wild-type and mutant forms of APPL were expressed in motoneurons to determine the effect of APPL at the neuromuscular junction (NMJ). We show that APPL was transported to motor axons and that its overexpression caused a dramatic increase in synaptic bouton number and changes in synapse structure. In an Appl null mutant, a decrease in the number of boutons was found. Examination of NMJs in larvae overexpressing APPL revealed that the extra boutons had normal synaptic components and thus were likely to form functional synaptic contacts. Deletion analysis demonstrated that APPL sequences responsible for synaptic alteration reside in the cytoplasmic domain, at the internalization sequence GYENPTY and a putative G(o)-protein binding site. To determine the likely mechanisms underlying APPL-dependent synapse formation, hyperexcitable mutants, which also alter synaptic growth at the NMJ, were examined. These mutants with elevated neuronal activity changed the distribution of APPL at synapses and partially suppressed APPL-dependent synapse formation. We propose a model by which APPL, in conjunction with activity-dependent mechanisms, regulates synaptic structure and number.

Glucocorticoid enhancement of dorsolateral striatum-dependent habit memory requires concurrent noradrenergic activity.

Previous findings indicate that post-training administration of glucocorticoid stress hormones can interact with the noradrenergic system to enhance consolidation of hippocampus- or amygdala-dependent cognitive/emotional memory. The present experiments were designed to extend these findings by examining the potential interaction of glucocorticoid and noradrenergic mechanisms in enhancement of dorsolateral striatum (DLS)-dependent habit memory. In experiment 1, different groups of adult male Long-Evans rats received training in two DLS-dependent memory tasks. In a cued water maze task, rats were released from various start points and were reinforced to approach a visibly cued escape platform. In a response-learning version of the water plus-maze task, animals were released from opposite starting positions and were reinforced to make a consistent egocentric body-turn to reach a hidden escape platform. Immediately post-training, rats received peripheral injections of the glucocorticoid corticosterone (1 or 3 mg/kg) or vehicle solution. In both tasks, corticosterone (3 mg/kg) enhanced DLS-dependent habit memory. In experiment 2, a separate group of animals received training in the response learning version of the water plus-maze task and were given peripheral post-training injections of corticosterone (3 mg/kg), the ß-adrenoreceptor antagonist propranolol (3 mg/kg), corticosterone and propranolol concurrently, or control vehicle solution. Corticosterone injections again enhanced DLS-dependent memory, and this effect was blocked by concurrent administration of propranolol. Propranolol administration by itself (3 mg/kg) did not influence DLS-dependent memory. Taken together, the findings indicate an interaction between glucocorticoid and noradrenergic mechanisms in DLS-dependent habit memory. Propranolol administration may be useful in treating stress-related human psychopathologies associated with a dysfunctional DLS-dependent habit memory system.

Dissociation of hippocampus and caudate nucleus memory systems by posttraining intracerebral injection of dopamine agonists.

The effect of posttraining intracerebral injections of the indirect dopamine (DA) agonist d-amphetamine, the direct D2 agonist LY 171555, and the direct D1 agonist SKF-38393 on the acquisition of two 8-arm radial maze tasks were examined. On a win-stay task, a light cue signaled the location of food in 4 randomly selected maze arms on each trial, and animals were required to visit each of the lit arms twice within a trial. Posttraining intracaudate injection of d-amphetamine (10.0 and 15.0 micrograms), LY 171555 (2.0 micrograms), and SKF-38393 (5.0 micrograms) all improved win-stay acquisition in relation to saline-injected controls. In contrast, posttraining intrahippocampal injection of DA agonists had no effect on win-stay acquisition. On a win-shift task, rats were allowed to obtain food from 4 randomly selected maze arms, followed by a delay period in which they were removed from the maze. They were returned to the maze for a retention test in which only those arms that had not been visited before the delay contained food. Posttraining intrahippocampal (but not intracaudate) injection of d-amphetamine (5.0 micrograms), LY 171555 (2.0 micrograms), and SKF-38393 (5.0 micrograms) all improved win-shift retention in relation to saline-injected controls. The results demonstrate a double dissociation of hippocampus and caudate nucleus memory functions and show that posttraining injection of both D1 and D2 agonists modulate the memory processes subserved by both hippocampus and caudate nucleus.

Double dissociation of fornix and caudate nucleus lesions on acquisition of two water maze tasks: further evidence for multiple memory systems.

The present study examined the effect of lesions of the caudate nucleus or fimbria-fornix on the acquisition of two water maze tasks. In both tasks, two rubber balls with different visual patterns were used as platforms (i.e., cues). The "correct" cue was attached to a submerged rectangular platform and could be mounted by an animal to escape the water. The "incorrect" cue was attached to a thin round pedestal and could not be mounted. In a spatial version of the task, the correct cue was located in the same quadrant of the maze on all trials, whereas the visual pattern on the cue was varied from trial to trial. Lesions of the fornix, but not the caudate nucleus, impaired acquisition of this spatial task in relation to control animals. In a simultaneous visual discrimination version of the task, the correct cue on all trials was one with a specific visual pattern, and the spatial location of the correct cue was varied from trial to trial. Lesions of the caudate nucleus, but not the fornix, impaired acquisition of this visual discrimination task in relation to control animals. The double dissociation observed supports the hypothesis that the hippocampus and caudate nucleus are parts of systems that differ in the type of memory they mediate.

Double dissociation of hippocampal and dorsal-striatal memory systems by posttraining intracerebral injections of 2-amino-5-phosphonopentanoic acid.

Rats received an 8-trial training session on a spatial or cued task in a water maze, followed by a posttraining intracerebral injection of AP5 or saline. On a retention test 24 hr later, latency to mount the escape platform was used as a measure of memory. Intrahippocampal (10 micrograms), but not intra-dorsal striatal (2, 5, or 10 micrograms), injection of AP5 impaired memory in the spatial task. In contrast, intra-dorsal striatal (2 micrograms), but not intrahippocampal (2, 5, or 10 micrograms) injection of AP5 impaired memory in the cued task. Intracerebral injections of AP5 delayed 2 hr posttraining were ineffective. The findings indicate a double dissociation of the roles of the hippocampus and dorsal striatum in memory, a role for N-methyl-D-aspartate receptor function in posttraining memory processes, and a glutamatergic modulation of both hippocampal and dorsal striatal memory processes, suggesting that different forms of memory may share a similar neurochemical basis.

Testosterone has rewarding affective properties in male rats: implications for the biological basis of sexual motivation.

Evidence from mammalian species, including humans, suggests that testosterone (T) enhances motivational aspects of sexual behavior, although the mechanism by which T exerts this effect is unknown. The hypothesis that increases in plasma T have rewarding affective properties was examined. Acute elevations of plasma T were induced in intact male rats by systemic administration of a recently developed testosterone-hydroxypropyl-beta-cyclodextrin inclusion complex that mimics pulsatile release of the hormone. In a conditioned-place-preference paradigm, rats displayed a preference for an environment previously paired with T administration (800 micrograms/kg and 1,200 micrograms/kg) as opposed to an environment paired with saline administration, indicating that T has rewarding affective properties. The findings suggest that T may enhance motivational aspects of mammalian sexual behavior by facilitating acquisition or expression of learned associations between environmental stimuli and sexual activity.

Rewarding affective properties of intra-nucleus accumbens injections of testosterone.

On alternating days, adult male Long-Evans rats implanted with bilateral cannulas in the nucleus accumbens received intracerebral injections of testosterone in a water-soluble cyclodextrin inclusion complex (0.125, 0.25, or 0.5 microg/0.5 microl saline) or saline immediately prior to being confined for 30 min to 1 of 2 compartments of a place-preference apparatus. All rats received 8 days of pairings (4 hormone and 4 saline). On Day 9 the rats were given a 20-min test session during which they had access to all compartments of the apparatus. No hormone was injected prior to the test session. On the test day, rats spent significantly more time in the compartment previously paired with bilateral intra-accumbens injections of testosterone (0.25 and 0.5 microg/0.5 microl saline) than in the compartment previously paired with saline injections. The findings indicate that intra-accumbens injections of testosterone are sufficient to produce reward.

Posttraining intrahippocampal estradiol injections enhance spatial memory in male rats: interaction with cholinergic systems.

Male Long-Evans rats received an 8-trial training session in a spatial water maze task, followed by a unilateral posttraining intrahippocampal injection of either estradiol (1.0 microgram/0.5 microliter) or saline. Retention was tested 24 hr later, and latency to escape was used as a measure of memory. Retention test escape latencies of rats given intrahippocampal injections of estradiol were lower than those of saline-treated rats, indicating an enhancement of memory. Intrahippocampal injections of estradiol delayed 2 hr posttraining did not affect retention. In Experiment 2, the memory enhancing effect of intrahippocampal injection of estradiol was blocked by peripheral administration of a subeffective dose (0.1 mg/kg) of the cholinergic antagonist scopolamine. Intrahippocampal injections of estradiol enhance memory in male rats, and estradiol may influence memory through an interaction with muscarinic cholinergic systems.

Place conditioning with dopamine D1 and D2 agonists injected peripherally or into nucleus accumbens.

The conditioned place preference technique was used to assess the affective properties of the direct dopamine D1 agonist, SKF38393, and the direct D2 agonist, LY171555 (quinpirole). A three compartment apparatus was used: the animals' pre-experimental preference for the two choice compartments was equal and, within each experimental group, half the rats received drug pairings in each choice compartment. Intraperitoneal injections of SKF38393 produced conditioned place aversions at all doses tested (1.0-4.0 mg/kg); LY171555 produced weak conditioned place preferences at 1.0 and 2.0 mg/kg, but no reliable effect at 4.0 mg/kg. Bilateral intra-accumbens microinjections of SKF38393 produced strong preferences at all doses tested (0.5-2.0 micrograms/side); LY171555 produced strong preferences at two doses (0.5 and 1.0 micrograms/side) and no effect at a third dose (2.0 micrograms/side). These results suggest that activation of either D1 or D2 receptors in the nucleus accumbens can produce reward, and that D1 receptors (and possibly also D2 receptors) located elsewhere in the brain or in the periphery may mediate aversive effects.

Bioactive lipids in excitatory neurotransmission and neuronal plasticity.

Long-term potentiation (LTP), a model of activity-dependent synaptic plasticity and of certain forms of memory, comprises the persistent enhancement of excitatory neurotransmission that results from high-frequency activation. A presynaptic component of LTP is thought to be modulated by a retrograde messenger generated by the postsynaptic neuron. Arachidonic acid, nitric oxide, carbon monoxide and PAF have each been proposed as retrograde messengers in LTP, but arachidonic acid, unlike PAF, requires NMDA receptor activation. A PAF antagonist (BN 52021) that provides neuroprotection in ischemia-reperfusion displaces [3H] PAF bound to presynaptic membranes, blocks PAF-induced glutamate exocytosis and inhibits LTP. An antagonist selective for the intracellular PAF binding site (BN 50730) did not affect LTP, nor did BN 52021 modify NMDA currents. LTP was induced with weak synaptic stimulation coupled with postsynaptically administered enzyme resistant mcPAF. Theta-burst stimulation (10 min) after bath applications of mcPAF (1 microM) induced APV-independent LTP that was blocked by 5 microM BN 52021. When this antagonist was infused into the hippocampus before or immediately after training, it impaired memory of inhibitory avoidance training in the rat. Memory was not altered if the antagonist is infused 30 or 60 min after training. Moreover, mcPAF enhances memory on retention test performance of step-down inhibitory avoidance habituation and learning in rats. Also, memory was studied using a caudate nucleus-dependent cued water maze task. Rats received an 8 trial (30 s intertrial interval) training session in which a visible cued escape platform was located in a different quadrant of the maze of each trial. Following trial 8, the rats received a unilateral post-training intra-caudate injection of mcPAF (1 microgram/0.5 microliter), BN 52021 (0.5 microgram/0.5 microliter) or vehicle. On a retention test session 24 h later, latency to mount the escape platform was used as a measure of memory. The retention test escape latencies of rats given mcPAF were significantly lower than those of the vehicle-injected controls, indicating a memory enhancing effect of mcPAF. Injection of mcPAF did not affect retention when administered 2 h post-training, indicating a time-dependent effect of mcPAF on memory. The latencies for animals injected with BN 52021 were significantly higher than those of the controls, indicating that antagonism of endogenous PAF impairs memory. The findings show that PAF plays a role in memory formation in a caudate-mediated cued discrimination task. Administration of BN 52021 2 h post-training had no affect on retention, indicating a time-dependent effect of endogenous PAF on memory formation. PAF, the most potent bioactive lipid known, modulates excitatory synaptic transmission, neuronal plasticity and memory. When PAF production is overstimulated as in seizures or ischemia, it becomes neurotoxic.

Intra-hippocampal estradiol infusion enhances memory in ovariectomized rats.

Ovariectomized adult Long-Evans rats received an eight-trial training session in a hippocampal-dependent hidden platform water maze task. Following trial 8, rats received an intra-hippocampal injection of estradiol in a water soluble cyclodextrin inclusion complex (1.0, 2.0 or 5.0 micrograms/0.5 microliter), or saline. Twenty-four hours later, the retention test escape latencies of rats administered post-training intra-hippocampal injections of estradiol (5.0 micrograms) were significantly lower than those of saline treated rats, indicating a memory-enhancing effect of estradiol. Injections of estradiol (5.0 micrograms) given 2 h post-training had no effect on retention, indicating a time-dependent effect of estradiol on memory storage processes.

Effects of peripherally injected vasopressin and des-glycinamide vasopressin on the extinction of a spatial learning task in rats.

An elevated eight-arm radial maze was employed to study the effects of neuropeptide administration on the spatial learning abilities of food-deprived rats. Following 18 days of reinforced training, each animal was briefly exposed to the maze with no food available in any of the eight food-cups. Immediately after this preliminary trial, animals were injected with a single subcutaneous dose of either saline, arginine vasopressin (AVP: 1.0 or 5.0 micrograms/kg), or an AVP analog with only weak endocrinological activity, des-gly-arginine vasopressin (DG-AVP: 1.0, 5.0 or 10.0 micrograms/kg). Additional extinction trials were conducted at 2, 4, 6 and 8 h post-injection. These tests consisted of individually placing an animal on the empty maze and recording the number of arms chosen in a 5-min period. In this situation, animals learn that food is no longer present in the maze and, consequently, extinguish responding. Vasopressin potentiated this radial maze extinction behavior while DG-AVP produced behavioral results directionally opposite to those predicted by a memory facilitation hypothesis. In a subsequent experiment, vasopressin had no effects on unconditioned locomotor activity measured 2 and 4 h post-injection. These results suggest that: vasopressin improved the learning that occurred during extinction of conditioned appetitive behaviors, these vasopressin effects on conditioned behavior were independent of any unconditioned, sedative or non-specific actions of the peptide, and peripheral endocrinological responses may be necessary to demonstrate memory-enhancing effects following peripherally administered AVP.

Amygdala modulates memory for changes in reward magnitude: reversible post-training inactivation with lidocaine attenuates the response to a reduction in reward.

The present study used a reward reduction paradigm to examine the role of the amygdala in memory for reduction in reward magnitude. Male Sprague-Dawley rats were implanted with bilateral amygdala cannulae and trained to run a straight alley (6 trials/day) for either ten or one 45-mg food pellets. On Day 10 of training, half the animals in the 10 pellet reward group were shifted to a one pellet reward. Immediately following shifted trials, the animals received an intra-amygdala injection of either a 2% lidocaine solution or phosphate buffer (0.5 microliter/side). Shifted training continued for 2 more days and no further injections were given. Shifted animals that received a buffer injection displayed a sharp increase in response latencies compared to unshifted controls on the second day of shifted training. In contrast, shifted animals that received intra-amygdala injections of lidocaine exhibited significantly lower latencies compared to the shifted vehicle group on the second day of shifted training. The findings indicate that post-training inactivation of the amygdala attenuates the response to reward reduction, suggesting that the amygdala modulates the storage for a reduction in reward magnitude.